Release of Growth Hormone from Purified Somatotrophs: Interrelation between Ca⁺⁺and Adenosine 3′,5′-Monophosphate*

Abstract

cAMP is thought to be an essential intracellular mediator in the release of GH from somatotrophs. Ca++ is required in the incubation medium to elicit GH release in vitro. We have carried out studies using a purified preparation of rat somatotrophs to see whether the Ca++ requirement procedes or follows the accumulation of cAMP induced by prostaglandin E2 (which increases adenylate cyclase activity) and 3-isobutyl-1-methylxanthine (a phosphodiesterase inhibitor). Incubation of somatotrophs in low Ca++ medium (less than 85 microM) abolished the release of GH induced by the two secretagogues, while the increase in intracellular cAMP was actually augmented. Thus, Ca++ is required in the incubation medium to express the action of intracellular cAMP.

Release of growth hormone from purified somatotrophs: effects of the calcium channel antagonists diltiazem and nifedipine on release induced by growth hormone-releasing factor

“…We attribute this to an increase in adenylate cyclase activity resulting from the putative decrease in cytosolic Ca2+. The observation that there is no reduction in the magnitude of the GWF-induced increase in cAMP reinforces our previous conclusion (Spence et al 1980;Kraicer and Spence 198 1;Kraicer and Chow 1982) that Ca2' is required at a step or steps after CAMP.…”

“…9 and 11) while values significantly different from GRF are indicated by "@". seen in our studies using low Ca2+ media (Spence et al 1980;cer et d. 198g2), where a number of secretagogues, including GRF, which increase cAMP accumulation, showed a further augmentation in cAMP accumulation in low Ca2+. We attribute this to an increase in adenylate cyclase activity resulting from the putative decrease in cytosolic Ca2+.…”

“…Earlier data indicated that an increase in cytosolic @a2+ is a requirement for augmented GH release induced by a number of secretagogues, and that this increase in cytosolic ca2+ might be derived from either increased uptake from the extracellular compartment, or from the movement of a "bound" intracellular pool to the cytosol (Sheppud et al 1980;Spence et al 1980;Kraicer and Spence 198 1 ;Kraicer and Chow 1982). Thus GH release is stimulated by high extracellular K+ or ca2+ ionsphores that increase CaZC uptake by the somatotrophs (Kraicer and Spence 1981 ;Kraicer and Chow 1982).…”

Ion Channels and Signaling in the Pituitary Gland

“…VIP/PACAP receptors are also present in mammalian melanotrophs (492), lactotrophs (54), and folliculostellate cells (493). Some eicosanoids may also signal through this pathway in pituitary cells (494). The lack of expression of typical G s -coupled receptors in other pituitary cell types does not mean that the cAMP signaling pathway is not operative.…”

A modulatory role for cyclic AMP in the control of thyrotrophin release: studies with forskolin and dibutyryl cyclic AMP

“…Synergism between these messenger systems has been described in pancreatic islet cells, platelets and smooth muscle (Rasmussen & Barrett, 1984), but there is increasing evidence for interaction between calcium and cAMP in the pitui¬ tary (Schrey, Brown & Ekins, 1978;Spence, Sheppard & Kraicer, 1980;Cronin et al 1984). There are various possible modes of interaction between messenger systems, and the mechanisms of these phenomena in thyrotrophs await further study to give a fuller understanding of the regulation of TSH secretion.…”